期刊
SCIENTIFIC REPORTS
卷 10, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41598-020-58449-x
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资金
- National Health and Medical Research Council (NHMRC) [APP1026070]
- Australian Postgraduate Award (APA)
- Schizophrenia Research Institute (NSW Ministry of Health, Australia)
- Schizophrenia Research Institute (NSW Ministry of Trade and Investment, Australia)
- NSW Ministry of Health, Office of Health and Medical Research
- National Health and Medical Research Council (Australia) [1117079]
- Neuroscience Research Australia Scholarship
People with schizophrenia exhibit deficits in inhibitory neurons and cognition. The timing of maternal immune activation (MIA) may present distinct schizophrenia-like phenotypes in progeny. We investigated whether early gestation [gestational day (GD) 10] or late gestation (GD19) MIA, via viral mimetic polyI:C, produces deficits in inhibitory neuron indices (GAD1, PVALB, SST, SSTR2 mRNAs) within cortical, striatal, and hippocampal subregions of male adult rat offspring. In situ hybridisation revealed that polyI:C offspring had: (1) SST mRNA reductions in the cingulate cortex and nucleus accumbens shell, regardless of MIA timing; (2) SSTR2 mRNA reductions in the cortex and striatum of GD19, but not GD10, MIA; (3) no alterations in cortical or striatal GAD1 mRNA of polyI:C offspring, but an expected reduction of PVALB mRNA in the infralimbic cortex, and; (4) no alterations in inhibitory markers in hippocampus. Maternal IL-6 response negatively correlated with adult offspring SST mRNA in cortex and striatum, but not hippocampus. These results show lasting inhibitory-related deficits in cortex and striatum in adult offspring from MIA. SST downregulation in specific cortical and striatal subregions, with additional deficits in somatostatin-related signalling through SSTR2, may contribute to some of the adult behavioural changes resulting from MIA and its timing.
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